This study develops a hypothesis on the origin and nature of spatial frequency lateralization that is grounded in the biology of the visual system, and demonstrates its potential validity using a neural network model. Computational experiments show that differences in the timing of development of the magnocellular and parvocellular systems coupled with asynchronous maturation of the hemispheres could result in the development of hard-wired asymmetry that biases the processing of spatial frequencies. The results provide evidence that this hard-wired asymmetry has the potential to explain both the absolute and the relative frequency lateralization effects observed in psychophysical experiments. This evidence is utilized to support a theoretical model that explains the relative frequency lateralization effect in terms of an interaction between task-driven spatial attention and eccentricity-dependent frequency lateralization. Both the computational model demonstrating the basis of asymmetric development and lateralized spatial frequency processing, and the theoretical model illustrating the basis of the relative frequency lateralization effect, are specified in terms of neural structures and processes in the visual system. Two theories previously developed at an abstract level, namely, the Hellige theory on lateralized spatial frequency development and the Ivry and Robertson Double Filtering by Frequency theory of relative frequency lateralization (as applied to the visual system) are effectively made operational by this biological specification.

The hard-wired asymmetry that develops in the computational experiments exhibits a hemispheric bias based primarily on spatial frequency. There is also evidence of a secondary bias related to the visual pathways. The pathway bias happens to be opposite in direction from that proposed by other researchers to explain temporal frequency lateralization effects observed in electrophysiological investigations on visual frequency processing. This contradiction is addressed by postulating that the electrophysiological lateralization effects arise from known anatomical asymmetries in the vicinity of the occipital poles rather than from actual processing differences. This contention is supported through computational modeling of the dipole potential-VEP wave relationship. The model results demonstrate that dipole asymmetry attributable to anatomical differences could produce the observed lateralization effects.